ArticleThe Journal of experimental medicine2001
CD4(+) T cells from lupus-prone mice are hyperresponsive to T cell receptor engagement with low and high affinity peptide antigens: a model to explain spontaneous T cell activation in lupus.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 108 citations in OpenAlex.
- Activation of circulating TFH17 cells associated with activated naive and double negative 2 B cell expansion, and disease activity in systemic lupus erythematosus patients.Arthritis research & therapy · 2024Article
- Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Advances in Understanding the Roles of CD244 (SLAMF4) in Immune Regulation and Associated Diseases.Frontiers in immunology · 2021Review
- The Role of β Cell Stress and Neo-Epitopes in the Immunopathology of Type 1 Diabetes.Frontiers in endocrinology · 2020Review
- Sex-Dependent Effects on Liver Inflammation and Gut Microbial Dysbiosis After Continuous Developmental Exposure to Trichloroethylene in Autoimmune-Prone Mice.Frontiers in pharmacology · 2020Article
- Lupus-like autoimmune disease caused by a lack of Xkr8, a caspase-dependent phospholipid scramblase.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Lys63-polyubiquitination by the E3 ligase casitas B-lineage lymphoma-b (Cbl-b) modulates peripheral regulatory T cell tolerance in patients with systemic lupus erythematosus.Clinical and experimental immunology · 2018Article
- Selective Loss of Signaling Lymphocytic Activation Molecule Family Member 4-Positive CD8+ T Cells Contributes to the Decreased Cytotoxic Cell Activity in Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Lpr-induced systemic autoimmunity is unaffected by mast cell deficiency.Immunology and cell biology · 2015Article
- SEA antagonizes the imatinib-meditated inhibitory effects on T cell activation via the TCR signaling pathway.BioMed research international · 2014Article
- Lupus autoimmunity altered by cellular methylation metabolism.Autoimmunity · 2013Article
- Reducing FLI1 levels in the MRL/lpr lupus mouse model impacts T cell function by modulating glycosphingolipid metabolism.PloS one · 2013Article
- IL-7Rαlow memory CD8+ T cells are significantly elevated in patients with systemic lupus erythematosus.Rheumatology (Oxford, England) · 2012Article
- Identification and characterization of a lupus suppressor 129 locus on chromosome 3.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- A lupus-susceptibility C57BL/6 locus on chromosome 3 (Sle18) contributes to autoantibody production in 129 mice.Genes and immunity · 2009Article
- Fas expression on antigen-specific T cells has costimulatory, helper, and down-regulatory functions in vivo for cytotoxic T cell responses but not for T cell-dependent B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Splenic phagocytes promote responses to nucleosomes in (NZB x NZW) F1 mice.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Cholera toxin B accelerates disease progression in lupus-prone mice by promoting lipid raft aggregation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Reduced receptor editing in lupus-prone MRL/lpr mice.The Journal of experimental medicine · 2007Article
- Dendritic cells from lupus-prone mice are defective in repressing immunoglobulin secretion.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Polyclonal CD4(+) T cell activation is characteristic of spontaneous lupus. As a potential explanation for this phenotype, we hypothesized that T cells from lupus-prone mice are intrinsically hyperresponsive to stimulation with antigen, particularly to those peptide ligands having a low affinity for the T cell receptor (TCR). To test this hypothesis, we backcrossed the alpha and beta chain genes of the AND TCR specific for amino acids 88-104 of pigeon cytochrome C (PCC) to the Fas-intact MRL/Mp(+)(Fas-lpr) and to the H-2(k)-matched control backgrounds B10.BR and CBA/CaJ (MRL.AND, B10.AND, and CBA.AND, respectively), and assessed naive CD4(+) TCR transgenic T cell activation in vitro after its encounter with cognate antigen and lower affinity altered peptide ligands (APLs). MRL.AND T cells, compared with control B10.AND and CBA.AND cells, proliferated more when stimulated with agonist antigen. More strikingly, MRL.AND T cells proliferated significantly more and produced more interleukin 2 when stimulated with the APLs of PCC 88-104, having lower affinity for the transgenic TCR. These results imply that one of the forces driving polyclonal activation of alpha/beta T cells in lupus is an intrinsically heightened response to peptide antigen, particularly those with low affinity for the TCR, independent of the nature of the antigen-presenting cell and degree of costimulation.
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